The risk of deep venous thrombosis and of pulmonary embolism is at least as high as in any other surgical condition. In our experience, 13 % of patients develop some form of thrombotic complication. SpeciÞc risk factors include central venous lines, prolonged bed rest, and an intense inßammatory state. Prophylaxis should be started from admission. Interruptions for surgery should be reduced to minimum and discussed with the surgical team.

Conclusion

The management of the critically ill thermally injured patient can be very complex. The treatment modalities can remain at times controversial, as there is a lack of high-level evidence. There have been many advances in the Þeld of the critical care of the thermally injured patient, which would beneÞt from largescale multicenter trials. This brief chapter highlights few of the important nuances in the care of these patients and places emphasis on the need for intricate support for the all organ systems in order to improve morbidity and mortality.

References

1. WHO (2002) A graphical overview of the global burden of injuries. The injury chart book, vol 29. WHO, Geneva

2. Herndon DN (2007) Treatment of infection in burns. In: Herndon DN (ed) Total burn care, 3rd edn. Saunders Elsevier, Philadelphia

3. Herndon DN, Tompkins RG (2004) Support of the metabolic response to burn injury. Lancet 363(9424):1895Ð1902

4. Jeschke MG et al (2012) Handbook of burns, vol 1. Springer, Wien New York

5. Kraft R et al (2012) Burn size and survival probability in paediatric patients in modern burn care: a prospective observational cohort study. Lancet 379(9820):1013Ð1021

6. Jeschke MG et al (2008) Pathophysiologic response to severe burn injury. Ann Surg 248(3):387Ð401

7. Williams FN et al (2009) The leading causes of death after burn injury in a single pediatric burn center. Crit Care 13(6):R183

8. Barrow RE, Jeschke MG, Herndon DN (2000) Early ßuid resuscitation improves outcomes in severely burned children. Resuscitation 45(2):91Ð96

9. Greenhalgh DG (2007) Burn resuscitation. J Burn Care Res 28(4):555Ð565

10. Greenhalgh DG (2010) Burn resuscitation: the results of the ISBI/ABA survey. Burns 36(2):176Ð182

11. Kraft R et al. (2012) Optimized ßuid management improves outcomes of pediatric burn patients. J Surg Res 2012 June 6 Epub Þrst

12. Wolf SE et al (1997) Mortality determinants in massive pediatric burns. An analysis of 103 children with > or = 80 % TBSA burns (> or = 70 % full-thickness). Ann Surg 225(5):554Ð565; discussion 565Ð569

13. Greenhalgh DG et al (2007) American Burn Association consensus conference to deÞne sepsis and infection in burns. J Burn Care Res 28(6):776Ð790

14. Latenser BA (2009) Critical care of the burn patient: the Þrst 48 hours. Crit Care Med 37(10):2819Ð2826

15. Pham TN, Cancio LC, Gibran NS (2008) American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res 29(1):257Ð266

16. Klein MB et al (2007) The association between ßuid administration and outcome following major burn: a multicenter study. Ann Surg 245(4):622Ð628

17. Rivers E et al (2001) Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345:1368Ð1377

18. Safße JI (2007) The phenomenon of Òßuid creepÓ in acute burn resuscitation. J Burn Care Res 28(3):382Ð395

19. Ivy ME et al (2000) Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 49(3):387Ð391

20. Faraklas I et al (2011) Colloid normalizes resuscitation ratio in pediatric burns. J Burn Care Res 32(1):91Ð97

21. Palmieri TL et al (2009) Inhalation injury in children: a 10 year experience at Shriners Hospitals for Children. J Burn Care Res 30(1):206Ð208

22. Sheridan RL, Hess D (2009) Inhaled nitric oxide in inhalation injury. J Burn Care Res 30(1):162Ð164

23. Endorf FW, Gamelli RL (2007) Inhalation injury, pulmonary perturbations, and ßuid resuscitation. J Burn Care Res 28(1):80Ð83

24. Erdman AR (2007) Is hydroxocobalamin safe and effective for smoke inhalation? Searching for guidance in the haze. Ann Emerg Med 49(6):814Ð816

25. Finnerty CC, Herndon DN, Jeschke MG (2007) Inhalation injury in severely burned children does not augment the systemic inßammatory response. Crit Care 11(1):R22

26. Barrow RE et al (2005) Mortality related to gender, age, sepsis, and ethnicity in severely burned children. Shock 23(6):485Ð487

27. Branski LK et al (2011) Transpulmonary thermodilution for hemodynamic measurements in severely burned children. Crit Care 15(2):R118

28. Kuntscher MV et al (2002) Transcardiopulmonary vs pulmonary arterial thermodilution methods for hemodynamic monitoring of burned patients. J Burn Care Rehabil 23(1):21Ð26

29. de Jonge E, Bos MM (2009) Patients with cancer on the ICU: the times they are changing. Crit Care 13(2):122

30. Gore DC et al (2003) Inßuence of fever on the hypermetabolic response in burn-injured children. Arch Surg 138(2):169Ð174; discussion 174

31. Hogan BK et al (2012) Correlation of American Burn Association sepsis criteria with the presence of bacteremia in burned patients admitted to the intensive care unit. J Burn Care Res 33(3):371Ð378

32. Murray CK et al (2007) Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg 142(7):639Ð642

33. Mosier MJ et al (2011) Early enteral nutrition in burns: compliance with guidelines and associated outcomes in a multicenter study. J Burn Care Res 32(1):104Ð109

34. Williams FN et al (2009) Modulation of the hypermetabolic response to trauma: temperature, nutrition, and drugs. J Am Coll Surg 208(4):489Ð502

35. Pereira C, Murphy K, Herndon D (2004) Outcome measures in burn care. Is mortality dead? Burns 30(8):761Ð771

36. Pereira CT et al (2006) Age-dependent differences in survival after severe burns: a unicentric review of 1,674 patients and 179 autopsies over 15 years. J Am Coll Surg 202(3):536Ð548

37. Jeschke MG et al (2011) Long-term persistance of the pathophysiologic response to severe burn injury. PLoS One 6(7):e21245

38. Jeschke MG (2009) The hepatic response to thermal injury: is the liver important for postburn outcomes? Mol Med 15(9Ð10):337Ð351

39. Price LA et al (2007) Liver disease in burn injury: evidence from a national sample of 31,338 adult patients. J Burns Wounds 7:e1

40. Jeschke MG et al (2011) Insulin protects against hepatic damage postburn. Mol Med 17(5Ð6):516Ð522

41. Gauglitz GG et al (2010) Post-burn hepatic insulin resistance is associated with endoplasmic reticulum (ER) stress. Shock 33(3):299Ð305

42. Song J et al (2009) Severe burn-induced endoplasmic reticulum stress and hepatic damage in mice. Mol Med 15(9Ð10):316Ð320

43. Jeschke MG et al (2009) Calcium and Er stress mediate hepatic apoptosis after burn injury. J Cell Mol Med 13:1857Ð1865

44. Jeschke MG, Mlcak RP, Herndon DN (2007) Morphologic changes of the liver after a severe thermal injury. Shock 28(2):172Ð177

45. Jeschke MG et al (2007) Changes in liver function and size after a severe thermal injury. Shock 28(2):172Ð177

46. Ivy ME et al (1999) Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 20(5):351Ð353

47. Baxter CR (1987) Metabolism and nutrition in burned patients. Compr Ther 13(1):36Ð42 48. Medlin S (2012) Nutrition for wound healing. Br J Nurs 21(12):S11ÐS12, S14Ð15

49. Kremer T et al (2010) High-dose vitamin C treatment reduces capillary leakage after burn plasma transfer in rats. J Burn Care Res 31(3):470Ð479

50.Tanaka H et al (2000) Reduction of resuscitation ßuid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study. Arch Surg 135(3):326Ð331

51. Chrysopoulo MT et al (1999) Acute renal dysfunction in severely burned adults. J Trauma 46(1):141Ð144

52. Jeschke MG et al (1998) Mortality in burned children with acute renal failure. Arch Surg 133(7):752Ð756

53. Kallinen O et al (2012) Multiple organ failure as a cause of death in patients with severe burns. J Burn Care Res 33(2):206Ð211

54. Holm C et al (1999) Acute renal failure in severely burned patients. Burns 25(2):171Ð178 55. Przkora R et al (2006) Body composition changes with time in pediatric burn patients.

J Trauma 60(5):968Ð971; discussion 971

56. Przkora R, Herndon DN, Suman OE (2007) The effects of oxandrolone and exercise on muscle mass and function in children with severe burns. Pediatrics 119(1):e109Ðe116

57. Jeschke MG et al (2005) Endogenous anabolic hormones and hypermetabolism: effect of trauma and gender differences. Ann Surg 241(5):759Ð767; discussion 767Ð768

58. Jeschke MG et al (2008) Gender differences in pediatric burn patients: does it make a difference? Ann Surg 248(1):126Ð136

59. Przkora R et al (2006) BeneÞcial effects of extended growth hormone treatment after hospital discharge in pediatric burn patients. Ann Surg 243(6):796Ð801; discussion 801Ð803

Response

Marc G. Jeschke

7.1Introduction

Advances in therapy strategies, based on improved understanding of resuscitation, enhanced wound coverage, more appropriate infection control, and improved treatment of inhalation injury, improved the clinical outcome of burn patients over the past years [1, 2]. However, severe burns remain a devastating injury affecting nearly every organ system and leading to significant morbidity and mortality [2]. One of the main contributors to adverse outcome of this patient population is the profound stress-induced hypermetabolic response, associated with severe alteration in glucose, lipid, and amino acid metabolism [1, 3–5] (Fig. 7.1).

M.G. Jeschke, MD, PhD, FACS, FCCM, FRCS(C)

Division of Plastic Surgery, Department of Surgery and Immunology, Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, University of Toronto,

Rm D704, Bayview Ave. 2075, M4N 3M5, Toronto, ON, Canada e-mail: marc.jeschke@sunnybrook.ca

Burn Wound

Fig. 7.1 Complexity of the post-burn hypermetabolic response. From Williams FN JACS 2009 April 208(4):489–502

7.2Post-Burn Hypermetabolism

A hallmark for severely burned patients is the hypermetabolic response that is not only very profound but also extremely complex and most likely induced by stress and inflammation [1, 3–5]. The cause of this response is not entirely defined, but it has been suggested that sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are involved in initiating the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state [6–15]. In addition, cytokines, endotoxin, neutrophil-adherence complexes, reactive oxygen species, nitric oxide, and coagulation as well as complement cascades have also been implicated in regulating this response to burn injury [16]. Once these cascades are initiated, their mediators and by-products appear to stimulate the persistent and increased metabolic rate associated with altered glucose, lipid, and amino acid metabolism seen after severe burn injury [17] (Fig. 7.1).

The metabolic changes post-burn occur in two distinct patterns of metabolic regulation following injury [18]:

1.The first phase occurs within the first 48 h of injury and has classically been called the “ebb phase” [18, 19], characterized by decreases in cardiac output,